000109085 001__ 109085
000109085 005__ 20230519145506.0
000109085 0247_ $$2doi$$a10.3390/jcm10153429
000109085 0248_ $$2sideral$$a125227
000109085 037__ $$aART-2021-125227
000109085 041__ $$aeng
000109085 100__ $$aGros, Mónica
000109085 245__ $$aNeurotransmitter Dysfunction in Irritable Bowel Syndrome: Emerging Approaches for Management
000109085 260__ $$c2021
000109085 5060_ $$aAccess copy available to the general public$$fUnrestricted
000109085 5203_ $$aIrritable bowel syndrome (IBS) is a functional gastrointestinal disorder whose aetiology is still unknown. Most hypotheses point out the gut-brain axis as a key factor for IBS. The axis is composed of different anatomic and functional structures intercommunicated through neurotransmitters. However, the implications of key neurotransmitters such as norepinephrine, serotonin, glutamate, GABA or acetylcholine in IBS are poorly studied. The aim of this review is to evaluate the current evidence about neurotransmitter dysfunction in IBS and explore the potential therapeutic approaches. IBS patients with altered colorectal motility show augmented norepinephrine and acetylcholine levels in plasma and an increased sensitivity of central serotonin receptors. A decrease of colonic mucosal serotonin transporter and a downregulation of α2 adrenoceptors are also correlated with visceral hypersensitivity and an increase of 5-hydroxyindole acetic acid levels, enhanced expression of high affinity choline transporter and lower levels of GABA. Given these neurotransmitter dysfunctions, novel pharmacological approaches such as 5-HT3 receptor antagonists and 5-HT4 receptor agonists are being explored for IBS management, for their antiemetic and prokinetic effects. GABA-analogous medications are being considered to reduce visceral pain. Moreover, agonists and antagonists of muscarinic receptors are under clinical trials. Targeting neurotransmitter dysfunction could provide promising new approaches for IBS management.
000109085 536__ $$9info:eu-repo/grantAgreement/ES/DGA/ARAINF-0567-2012$$9info:eu-repo/grantAgreement/ES/DGA-FEDER/A02-17R
000109085 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000109085 590__ $$a4.964$$b2021
000109085 592__ $$a1.04$$b2021
000109085 594__ $$a4.4$$b2021
000109085 591__ $$aMEDICINE, GENERAL & INTERNAL$$b55 / 172 = 0.32$$c2021$$dQ2$$eT1
000109085 593__ $$aMedicine (miscellaneous)$$c2021$$dQ1
000109085 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000109085 700__ $$0(orcid)0000-0002-0061-7989$$aGros, Belén$$uUniversidad de Zaragoza
000109085 700__ $$0(orcid)0000-0003-4758-3998$$aMesonero, José Emilio$$uUniversidad de Zaragoza
000109085 700__ $$0(orcid)0000-0002-5797-3909$$aLatorre, Eva$$uUniversidad de Zaragoza
000109085 7102_ $$11012$$2410$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Fisiología
000109085 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000109085 7102_ $$11002$$2050$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Biología Celular
000109085 773__ $$g10, 15 (2021), 3429 [22 pp.]$$pJ. clin.med.$$tJournal of Clinical Medicine$$x2077-0383
000109085 8564_ $$s985440$$uhttps://zaguan.unizar.es/record/109085/files/texto_completo.pdf$$yVersión publicada
000109085 8564_ $$s2739120$$uhttps://zaguan.unizar.es/record/109085/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000109085 909CO $$ooai:zaguan.unizar.es:109085$$particulos$$pdriver
000109085 951__ $$a2023-05-18-15:06:13
000109085 980__ $$aARTICLE